lithium: Potential Neuroprotective Methods
Although great advances have been made in understanding lithium and other psychopharmaceuticals, the neuroprotective effect of lithium is still being researched.[1]
It is possible that the increased permeability allows in chemicals which could increase acidity, which itself has a correlation with Alzheimer's[6] (possibly because acidity encourages damage to cells which allows more free radical copper and iron loose in the body, and is inflammatory), and thereby encourage creation of amyloid plaque, thereby giving lithium a double neuroprotective effect.
Research already shows that the level of lithium in the brain is greater than in the blood in some older people. This could be the blood brain barrier becoming too strong, trapping lithium in the brain. It is suggested to reduce the level of lithium to treat the patient rather than to respond to the serum level as a result.[7] Does this only happen in long-term users of lithium? Could long-term zinc deficiency from taking lithium, probably used in the course of lithium mechanisms of protecting the brain and controlling mania have this result?
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©Deborah Barges August 2020 open access
One thing that could cause a neuroprotective effect would be increasing the pH, or alkalinity, of the brain. It turns out that an alkaline brain builds less plaque, protecting from Alzheimer's.[2]
Another possible cause of neuroprotection would be the reduction of zinc, which increases the blood-brain barrier, and could protect it from neurotoxins. Amyloid plaque has been found in at least some cases to contain zinc, copper, and iron.[3] Copper and iron are free radicals, and zinc is used by the body to remove copper from the body, a copper antagonist.[4] It is possible however that in the process of protecting the brain from copper, it is actually increasing damage to the brain by increasing the permeability of the blood-brain barrier.[5] That may be on purpose, to remove the copper, but if seems not to be a complete benefit.
It is possible that the increased permeability allows in chemicals which could increase acidity, which itself has a correlation with Alzheimer's[6] (possibly because acidity encourages damage to cells which allows more free radical copper and iron loose in the body, and is inflammatory), and thereby encourage creation of amyloid plaque, thereby giving lithium a double neuroprotective effect.
Research already shows that the level of lithium in the brain is greater than in the blood in some older people. This could be the blood brain barrier becoming too strong, trapping lithium in the brain. It is suggested to reduce the level of lithium to treat the patient rather than to respond to the serum level as a result.[7] Does this only happen in long-term users of lithium? Could long-term zinc deficiency from taking lithium, probably used in the course of lithium mechanisms of protecting the brain and controlling mania have this result?
These are areas that could be researched, if such research is not already being done.
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©Deborah Barges August 2020 open access
